However compensatory hypertrophy after myocardial infarction is temporary. In the end, cardiac dilation and myocardium thinning occurs and heart function is further deteriorated. Angiogenesis is very important to preserve adapt cardiac hypertrophy and contractile function. Neo-vascular could support more oxygen and energy to hypertrophic myocardium in nonischemic zone. When oxygen and energy support is insufficient for hypertrophical myocytes, apoptosis or/and necrosis of cell would occur, leading to myocardium thinning and cardiac contractile impairment. Therefore, relatively insufficient microvessel is a key pathological feature in the transition from adaptive cardiac hypertrophy to cardiac dysfunction. Integrin linked kinase is a serine/threonine protein kinase, as a downstream kinase of b- integrin. It is an important component of mechanical stretch sensor, which can transduce mechanical signal to intra-cellular biomechanical signals,Levatin and initiate a serial of cellular responses. When cardiac pre-load increased, ILK is thought to transduce cardiac pressure load into a cellular compensatory growth program via activation of the Rho family guanine triphosphatases, ras-related C3 botulinum toxin substrate 1 and Cell division control protein 42. ILK is also observed to promote vascular development and angiogenesis. In ILK knockout mice and zebrafish, the vasculature formation is markedly abnormal. Vascular endothelial growth factor was identified as downstream of ILK to induce tissue angiogenesis. Several study revealed ILK was involved in cancer cell VEGF expression and tumor angiogenesis. In our pervious work, overexpression of ILK after myocardial infarction can significantly induced myocardium hypertrophy and tissue angiogenesis to improve heart function. However the patholo-physiological role of ILK in cardiac remodeling after MI has not been clear. Whether impairment of ILK related signaling pathway is the key feature for transition from adaptive cardiac hypertrophy to cardiac dysfunction needs to be clarified. To this aim, we assessed time-dependent ILK expression in non-ischemic myocardium after MI. We observed ILK as well as its related proangiogenic signaling down-regulated Crovatin during the transition from adaptive cardiac hypertrophy to cardiac dysfunction; while the sustained ILK expression could maintain responsible angiogenesis in myocardium and improve heart function. Before sacrificed transthoracic echocardiography and cardiac catheterization were performed to evaluate heart function. To evaluate the therapeutic effect of sustained ILK expression in cardiac remodeling, 19 rats underwent MI and were enrolled in study. 4 weeks after MI, the rats were thoracotomy again. Ad-ILK or Ad-null was injected into remote myocardium randomly and 12 rats were survived from the operation. Two weeks after operation, we measured heart function by ECG, and executed rats to harvest myocardium for western blot analysis. Angiogenesis pathway was down-regulated in non-ischemic myocardium 8 weeks post MI. Furthermore we assessed the microvessel density by histological analysis. von Willebrand factor was selected as endothelial cell biomarker in immunestaining. In peri-infarct zone, microvascular density was significantly increased in the MI group compared with sham group. No difference of microvessel density was observed among three time points after MI. In remote zone, microvessel density was moderately increased after MI, but not reached significantly difference compared with sham. In rats executed 8 weeks after MI, the microvessel density was significantly decreased compared with those in rats executed other time spots after MI.